Готові списки джерел за темами / Neurotoxicity assessment

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Добірка наукової літератури з теми "Neurotoxicity assessment"

Автор: Grafiati

Опубліковано: 13 вересня 2022

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Статті в журналах з теми "Neurotoxicity assessment"

Kulig, Beverly M. "Comprehensive Neurotoxicity Assessment." Environmental Health Perspectives 104 (April 1996): 317. http://dx.doi.org/10.2307/3432651.

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Kulig, B. M. "Comprehensive neurotoxicity assessment." Environmental Health Perspectives 104, suppl 2 (April 1996): 317–22. http://dx.doi.org/10.1289/ehp.96104s2317.

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Parng, Chuenlei, Nicole Marie Roy, Christopher Ton, Yingxin Lin, and Patricia McGrath. "Neurotoxicity assessment using zebrafish." Journal of Pharmacological and Toxicological Methods 55, no. 1 (January 2007): 103–12. http://dx.doi.org/10.1016/j.vascn.2006.04.004.

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GREENBERG, B. D., P. A. MOORE, R. LETZ, and E. L. BAKER. "Computerized Assessment of Human Neurotoxicity." Survey of Anesthesiology 30, no. 4 (August 1986): 189. http://dx.doi.org/10.1097/00132586-198608000-00010.

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Boyes, William K., Michael L. Dourson, Jacqueline Patterson, Hugh A. Tilson, William F. Sette, Robert C. MacPhail, Abby A. Li, and John L. O'Donoghue. "EPA's Neurotoxicity Risk Assessment Guidelines." Toxicological Sciences 40, no. 2 (1997): 175–84. http://dx.doi.org/10.1093/toxsci/40.2.175.

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Boyes, W. "EPA's Neurotoxicity Risk Assessment Guidelines, ,." Fundamental and Applied Toxicology 40, no. 2 (December 1997): 175–84. http://dx.doi.org/10.1006/faat.1997.2388.

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Kodell, R. L., J. J. Chen, and D. W. Gaylor. "Neurotoxicity Modeling for Risk Assessment." Regulatory Toxicology and Pharmacology 22, no. 1 (August 1995): 24–29. http://dx.doi.org/10.1006/rtph.1995.1064.

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Jacobson, Joseph L., and Sandra W. Jacobson. "Prospective, Longitudinal Assessment of Developmental Neurotoxicity." Environmental Health Perspectives 104 (April 1996): 275. http://dx.doi.org/10.2307/3432647.

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Jacobson, J. L., and S. W. Jacobson. "Prospective, longitudinal assessment of developmental neurotoxicity." Environmental Health Perspectives 104, suppl 2 (April 1996): 275–83. http://dx.doi.org/10.1289/ehp.96104s2275.

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Giardina, William J. "Assessment of temafloxacin neurotoxicity in rodents." American Journal of Medicine 91, no. 6 (December 1991): S42—S44. http://dx.doi.org/10.1016/0002-9343(91)90310-t.

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Дисертації з теми "Neurotoxicity assessment"

Ray, Maria A. "Behavioral assessment of neurotoxicity and fatigue during chemotherapy in mice /." Available to subscribers only, 2008. http://proquest.umi.com/pqdweb?did=1597629831&sid=1&Fmt=2&clientId=1509&RQT=309&VName=PQD.

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Анотація:

Thesis (M.S.)--Southern Illinois University Carbondale, 2008.
"Department of Medical Microbiology, Immunology and Cell Biology." Includes bibliographical references (p. 78-108). Also available online.

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Joshi, Pranav. "Three-Dimensional Human Neural Stem Cell Culture for High-Throughput Assessment of Developmental Neurotoxicity." Cleveland State University / OhioLINK, 2019. http://rave.ohiolink.edu/etdc/view?acc_num=csu155965254496159.

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Stengel, Daniel [Verfasser], and Thomas [Akademischer Betreuer] Braunbeck. "Development and validation of a neurotoxicological test battery for neurotoxicity risk assessment / Daniel Stengel ; Betreuer: Thomas Braunbeck." Heidelberg : Universitätsbibliothek Heidelberg, 2016. http://d-nb.info/1180616065/34.

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Abulhaija, Ashraf. "The Relationship Between Total Neuropathy Score-reduced, Neuropathy Symptoms and Function." Scholar Commons, 2017. http://scholarcommons.usf.edu/etd/6992.

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Chemotherapy Induced Peripheral Neuropathy (CIPN) is a common problem among cancer patients who receive a wide range of chemotherapy. This problem causes a decline in quality of life and increased disabilities. CIPN assessment instruments are either subjective, objective, or a combination of both. So far, there is no agreement on the best way for assessment. The goal of this study was to explore the relationships among subjective and objective CIPN assessment instruments. Specifically, this study aimed to 1) evaluate the relationship between the Total Neuropathy Score-reduced (mainly objective) and patients’ function, as measured by the interference scale of the Chemotherapy-Induced Peripheral Neuropathy Assessment Tool (subjective); and 2) evaluate the relationship between the Total Neuropathy Score-reduced and neuropathy symptom experience, as measured by the symptom experience scale of the Chemotherapy-Induced Peripheral Neuropathy Assessment Tool (Subjective). To achieve those aims, a secondary data analysis for 56 participants who participated in a study entitled: Group Acupuncture for Treatment of Neuropathy from Chemotherapy was done. After Pearson correlations were calculated, the study found that there is a positive, weak relationship between the TNSr and the symptom experience scale of the CIPNAT(r=0.34). A positive, week relationship was found between the TNSr and the interference with activity scale of the CIPNAT(r=0.28). These results suggest that objective and subjective assessment are not highly correlated, and likely measure different aspects of CIPN. A comprehensive assessment approach is needed for decision making in the clinical oncology setting.

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Fournier, Kevin. "Construction d'indicateurs de toxicites cumulees : cas des composes organiques semi volatils dans les environnements interieurs." Thesis, Rennes 1, 2015. http://www.theses.fr/2015REN1B019/document.

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Les composés organiques semi volatils (COSV) sont largement présents dans les environnements intérieurs et sont suspectés d’être repro- ou neurotoxiques, mais peu de données sont disponibles quant à leur toxicité en mélanges. L’objectif de cette thèse est de proposer des indicateurs de toxicité cumulés pour les COSV détectés dans les logements français, dans un cadre d’évaluation des risques sanitaires cumulés. Les COSV ont été regroupés en fonction de leurs modes d’action communs, en lien avec les effets reprotoxiques (diminution de la concentration de testostérone sérique) et neurotoxiques (diminution de la viabilité neuronale). Des benchmark doses (BMD) ont ensuite été estimées par modélisation (modèle de Hill, PROAST, RIVM) des relations dose-réponse de la littérature décrivant la réponse d’intérêt. Des BMD comparables ont pu être estimées seulement pour 6 des 19 COSV reprotoxiques induisant une diminution de testostérone de 10 ou 50 % chez le rat adulte exposé par voie orale. Les facteurs de toxicité relatifs (RPF) estimés à partir des BMD sont sensiblement les mêmes en fonction du niveau de réponse (de 1600 pour le B(a)P à 0,1 pour le BBP), excepté pour le biphénol A qui passe de 7E+6 à 180. Considérant la mort neuronale in vitro, des BMD ont pu être estimées pour 13 COSV neurotoxiques, à partir de données provenant de différentes lignées et espèces. Les BMD équivalent à un niveau de réponse de 10 % s’échelonnent de 0,07 (PCB-153) à 95 µM (diazinon). L’originalité de ce travail repose sur le regroupement de composés de familles chimiques différentes qui constituent des contaminations réelles de notre environnement. Si l’estimation des quelques BMD a été possible à partir des données de la littérature, de nombreuses limites méthodologiques conduisent à émettre des recommandations en particulier sur la standardisation des protocoles expérimentaux et la disponibilité des résultats sous une forme adaptée à la modélisation de la relation dose-réponse
Semi-volatile organic compounds (SVOCs) are widely present in indoor environments and are suspected to be repro- or neurotoxic but little is known on the health impact on SVOC mixtures. The objective of this work is to derive cumulative toxicity indicators for SVOCs detected in French dwellings in carrying forward a cumulative health risk assessment. SVOCs were grouped according to their repro- and neurotoxic common modes of action (i.e. decrease in serum testosterone concentrations, decrease in neuronal viability). Benchmark doses (BMDs) were then estimated by modeling dose-response relationships from scientific literature (Hill models, PROAST, RIVM). Comparable BMDs were estimated only for 6 of the 19 reprotoxic SVOCs which are responsible to 10 or 50% decrease in testosterone in adult male rats orally exposed. Estimated relative potency factors (RPFs) from BMDs are similar according to the response level (from 1600 for the B(a)P to 0.1 for the BBP), excepted for bisphenol A moving from 7E+6 to 180. For in vitro neuronal death, BMDs were estimated for 13 neurotoxic SVOCs using data from different cell lines and species. BMDs equivalent to a 10% of response range from 0.07 (PCB-153) to 95 µM (diazinon). The originality of this work is the grouping of compounds from different chemical families which we are really exposed to. BMDs estimation from published data was possible but many methodological limitations lead us to put forward recommendations especially on the standardization of experimental protocols and the availability of results in adapted format for dose-response relationship modeling

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Lee, Iwa. "Developmental neurotoxicity of persistent and non-persistent pollutants : Behavioral and neurochemical assessments of a perfluorinated compound, pesticides and interaction effects." Doctoral thesis, Uppsala universitet, Institutionen för organismbiologi, 2015. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-261742.

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The focus of this thesis was to investigate developmental neurotoxic effects of different persistent and non-persistent environmental pollutants, alone or in binary mixtures, when exposure occurs during a critical period of brain development, in mice. The compounds investigated included a perfluorinated compound, perfluorohexane sulphonate (PFHxS), and four different pesticides, endosulfan, cypermethrin, chlorpyrifos and carbaryl. Both persistent and non-persistent pollutants are detected in the environment and in humans, which shows that exposure to these compounds is occurring in real life. Humans can therefore be exposed to various pollutants during their whole lifetime, starting from the gestational period to adulthood. Furthermore, exposure to environmental pollutants is rarely exclusive to a single compound, but rather occurs through combinations of various pollutants present in the environment. Exposure to environmental pollutants during human brain development have been suggested to be a possible cause for neuropsychiatric disorders, such as autism spectrum disorder (ASD) and attention deficit hyperactivity disorder (ADHD). Previous studies have shown that chemicals can induce irreversible disorders in brain function when exposure to these chemicals occurs during a critical defined period of the brain development known as the brain growth spurt (BGS). The BGS is characterized by a rapid growth and development of the immature brain. In humans, and mice, this period also overlaps the lactation period indicating that newborns and toddlers can be exposed via mothers’ milk as well. This thesis has shown that a single oral exposure to PFHxS, endosulfan, cypermethrin, chlorpyrifos or carbaryl can induce developmental neurotoxic effects in mice, when exposure occurs during a critical period of brain development. These effects are manifested as persistent altered adult spontaneous behavior in a novel home environment, modified habituation, altered susceptibility of the cholinergic system and changed levels of neuroproteins in the mouse brain. Furthermore, a single neonatal co-exposure to a binary mixture of carbaryl/chlorpyrifos or PFHxS/endosulfan can interact and exacerbate the adult behavioral effects. These effects were seen at dosages were the single compound did not elicit a response or induced a much weaker behavioral effect. This indicates that risk assessments conducted on single compounds might underestimate interaction effects of mixtures when co-exposed.

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De, Conto Véronique. "Importance du microenvironnement dans les modèles cérébraux in vitro pour le criblage phénotypique." Thesis, Université de Lille (2018-2021), 2021. http://www.theses.fr/2021LILUS046.

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Environ 90% des candidats-médicaments échouent en phase clinique, pour des raisons d’efficacité ou de toxicité qui impliquent souvent le système nerveux central (SNC). Ce fort taux d’échec souligne un manque de pertinence des modèles expérimentaux utilisés en amont, dont les modèles in vitro de cellules humaines. En effet, ces derniers ne prennent pas en compte toute la complexité du SNC, où les neurones organisés en 3 dimensions (3D) interagissent avec leur microenvironnement composé de cellules, de facteurs solubles et des molécules de la matrice extracellulaire (MEC). Les objectifs de ce travail étaient i) d’étudier l’influence de ces trois composantes du microenvironnement sur les cellules neuronales dans des modèles cérébraux in vitro par imagerie cellulaire automatisée, et ii) de développer des modèles cérébraux in vitro plus pertinents pour évaluer les effets neurotoxiques ou thérapeutiques de molécules par criblage phénotypique, notamment dans le cadre de la maladie de Parkinson (MP).Dans un premier temps, la technologie BIOMIMESYS® Brain a été développée. Cette matrice à base d’acide hyaluronique permet de mimer la MEC et de cultiver des cellules cérébrales en 3D dans des plaques 96 puits. La sensibilité des cellules Luhmes, une lignée de neurones dopaminergiques, aux inducteurs de la MP a été étudiée : les cellules ont montré une sensibilité plus faible dans BIOMIMESYS® Brain qu’en 2 dimensions (2D). Cette différence a pu être expliquée par deux phénomènes : une rétention partielle des molécules toxiques dans la matrice, et un phénotype de neurone dopaminergique moins mature qu’en 2D. L’importance du microenvironnement cellulaire a ensuite été étudiée au travers d’une co-culture de cellules Luhmes et d’astrocytes primaires humains en 2D. Cette co-culture a ensuite été transposée dans la matrice BIOMIMESYS®, formant ainsi un modèle complexe incluant à la fois le microenvironnement glial et le microenvironnement matriciel.En parallèle, l’influence du microenvironnement moléculaire a été étudiée sur les cellules SH-SY5Y, une lignée cellulaire issue d’un neuroblastome, couramment utilisée pour évaluer la neurotoxicité de molécules. Dans cette étude, les 24 principaux milieux décrits dans la littérature pour différencier ces cellules en neurones ont été criblés. Les 3 conditions les plus différenciantes en matière de ralentissement de la prolifération cellulaire et de croissance des neurites ont été sélectionnées : l’acide rétinoïque, la staurosporine, et l’Adénosine Monophosphate cyclique (AMPc) associée à du supplément B21. L’expression de marqueurs protéiques neuronaux et la sensibilité des cellules à des composés de toxicités connues ont été mesurées, en 2D et en 3D dans BIOMIMESYS® Brain. La maturité neuronale et la sensibilité aux composés neurotoxiques différaient selon le milieu, en étant les plus hautes en milieu B21+AMPc. La culture en 3D modifiait aussi la réponse des cellules, avec une sensibilité plus faible comparée aux cellules cultivées en 2D.Cette thèse a mis en évidence que le microenvironnement des neurones, qui inclut la MEC, les cellules gliales et les facteurs solubles, modifie la réponse neuronale in vitro et devrait par conséquent être considéré avec attention dans la recherche académique comme industrielle, dès les étapes de criblage de nouveaux médicaments
About 90% of drug candidates fail in clinical trials, for efficacy- and toxicity-related reasons, which often involve the Central Nervous System (CNS). This high failure rate highlights a lack of relevance in experimental models used upstream, including human in vitro models. Indeed, they do not take into account the complexity of the CNS, in which neurons are organized in 3 dimensions (3D) and interact with their microenvironment, composed of cells, soluble factors and extracellular matrix (ECM). The objectives of this PhD were i) to study the influence of these three microenvironment components on neuronal cells in cerebral in vitro models by automatized cellular imaging, and ii) to develop more relevant cerebral in vitro models for phenotypic screening, to assess neurotoxic or therapeutic effects, in the frame of Parkinson’s Disease (PD).First, the BIOMIMESYS® Brain technology has been developed. This acid hyaluronic based-matrix allows the simulation of the ECM and a 3D culture of cerebral cells in 96-well plates. The sensitivity of Luhmes cells, a dopaminergic neuronal cell line, to PD inducers has been studied: the cells displayed a lower sensitivity in BIOMIMESYS® Brain compared to cells cultured in 2 dimensions (2D). This difference was explained by two phenomena: a partial retention of toxic molecules in the matrix, and a lower neuronal maturity compared to cells cultured in 2D.The importance of the cellular microenvironment has been studied through a co-culture of Luhmes cells and primary human astrocytes in 2D. This co-culture has then been transposed in BIOMIMESYS® matrix, to form a complex model including both the glial and the matricial microenvironments.In parallel, the influence of the molecular microenvironment has been studied on the SH-SY5Y cells, a cell line derived from a neuroblastoma, commonly used for neurotoxicity assessment. In this study, the 24 major differentiation media described in the literature to differentiate these cells into neurons have been screened. The 3 most differentiating conditions in terms of proliferation slowdown and neurite elongation have been selected: retinoic acid, staurosporine, and cyclic Adenosine Monophosphate (cAMP) combined to B21 supplement. The neuronal protein marker expression and the cell sensitivity to compounds of known-toxicity have been measured, in 2D and in 3D in BIOMIMESYS® Brain. Both maturity and sensitivity of these neurons varied according to the differentiation medium, and were higher in B21+cAMP. The 3D cell culture modified also the cell response, with a lower sensitivity of cells cultured in 2D.This PhD highlighted that the microenvironment of neurons, including the ECM, the glial cells and the soluble factors, can modify the neuronal response in vitro, and should thus be considered carefully in academic research and as early as possible in the drug discovery industrial process

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Nixdorff, K., T. Borisova, S. Komisarenko, and Malcolm R. Dando. "Dual-use nano-neurotechnology: An assessment of the implications of trends in science and technology." 2018. http://hdl.handle.net/10454/16694.

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No
The chemical and biological nonproliferation regime stands at a watershed moment, when failure seems a real possibility. After the unsuccessful outcome of the 2016 Eighth Review Conference, the future of the Biological and Toxin Weapons Convention is uncertain. As the Chemical Weapons Convention (CWC) approaches its Fourth Review Conference in 2018, it has almost completed removing the huge stocks of chemical weapons, but it now faces the difficult organizational task of moving its focus to preventing the reemergence of chemical weapons at a time when the international security situation appears to be increasingly more difficult and dangerous. In this article, we assess the current and near-term state (5–10 years) and impact of three related areas of science and technology that could be of dual-use concern: targeted delivery of agents to the central nervous system (CNS), particularly by means of nanotechnology; direct impact of nanomaterials on synaptic functions in the CNS; and neuronal circuits in the brain that might be targeted by those with hostile intent. We attempt to assess the implications of our findings, particularly for the consideration of the problem of state-level interest in so-called nonlethal incapacitating chemical agents for law enforcement at the CWC Review Conference in 2018, but also more generally for the longer-term future of the chemical and biological nonproliferation regime.

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Книги з теми "Neurotoxicity assessment"

Harry, Jean. Neurotoxicity risk assessment for human health: Principles and approaches. Geneva: World Health Organization, 2001.

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Programme, United Nations Environment. Principles and methods for the assessment of neurotoxicity associated with exposure to chemicals. Geneva: World Health Organization ; Albany, NY : WHO Publications Center USA [distributor], 1986.

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United States. Environmental Protection Agency. Risk Assessment Forum, ed. Guidelines for neurotoxicity risk assessment. Washington, DC: Risk Assessment Forum, U.S. Environmental Protection Agency, 1998.

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(Producer), WHO, ed. Neurotoxicity Risk Assessment: Environmental Health Criteria Series No. 223 (Environmental Health Criteria). World Health Organisation, 2001.

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Principles and Methods for the Assessment of Neurotoxicity Associated With Exposure to Chemicals (Environmental Health Criteria Ser :No.60). World Health Organization, 1986.

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Частини книг з теми "Neurotoxicity assessment"

O’Byrne, Muriel, K. Tipton, G. McBean, and H. Kollegger. "Assessment of neurotoxicity and “neuroprotection”." In Advances in Research on Neurodegeneration, 153–64. Vienna: Springer Vienna, 1997. http://dx.doi.org/10.1007/978-3-7091-6842-4_15.

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Scallet, Andrew C., and William Slikker. "Biomarkers of Developmental Neurotoxicity." In Risk Assessment of Prenatally-Induced Adverse Health Effects, 63–77. Berlin, Heidelberg: Springer Berlin Heidelberg, 1992. http://dx.doi.org/10.1007/978-3-642-77753-0_4.

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Atterwill, C. "Current trends for the assessment of neurotoxicity in vitro." In Ersatz- und Ergänzungsmethoden zu Tierversuchen, 40–48. Vienna: Springer Vienna, 1997. http://dx.doi.org/10.1007/978-3-7091-6833-2_6.

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Salvo, Hope, and Mark T. Butt. "Regulatory Guide to the Histopathological Assessment of Neurotoxicity Studies." In Fundamental Neuropathology for Pathologists and Toxicologists, 519–35. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2011. http://dx.doi.org/10.1002/9780470939956.ch34.

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Hill, Bridgett N., Kayla D. Coldsnow, Deborah L. Hunter, Joan M. Hedge, David Korest, Kimberly A. Jarema, and Stephanie Padilla. "Assessment of Larval Locomotor Activity for Developmental Neurotoxicity Screening." In Neuromethods, 327–51. New York, NY: Springer US, 2021. http://dx.doi.org/10.1007/978-1-0716-1637-6_15.

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Ehrich, Marion, and David C. Dorman. "Predictive Value of In Vitro Systems for Neurotoxicity Risk Assessment." In In Vitro Neurotoxicology, 29–40. Totowa, NJ: Humana Press, 2004. http://dx.doi.org/10.1385/1-59259-651-7:29.

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Weiss, Dieter G. "Neurotoxicity Assessment by Recording Electrical Activity from Neuronal Networks on Microelectrode Array Neurochips." In Neuromethods, 467–80. Totowa, NJ: Humana Press, 2011. http://dx.doi.org/10.1007/978-1-61779-077-5_24.

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Shikuev, Alexey V., Taras A. Skoromets, Dmitri I. Skulyabin, Miroslav M. Odinak, and Alexander A. Skoromets. "Chapter 9. Feasibility Studies of Neurotoxicity Biomarkers for Assessment of Traumatic Brain Injury." In Biomarkers for Traumatic Brain Injury, 148–63. Cambridge: Royal Society of Chemistry, 2012. http://dx.doi.org/10.1039/9781849734745-00148.

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"Assessment of Neurotoxicity." In Animal Clinical Chemistry, 243–54. CRC Press, 2009. http://dx.doi.org/10.1201/9781420080124.ch11.

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"- Neurotoxicity of Nanomaterials." In Handbook of Safety Assessment of Nanomaterials, 428–59. Jenny Stanford Publishing, 2014. http://dx.doi.org/10.1201/b15668-16.

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Тези доповідей конференцій з теми "Neurotoxicity assessment"

Al-dosari, Aldana, Nadin Younes, and Gheyath Nasrallah. "Ecotoxicological assessment of two surfactant on the emryonic development." In Qatar University Annual Research Forum & Exhibition. Qatar University Press, 2021. http://dx.doi.org/10.29117/quarfe.2021.0149.

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In this study, zebrafish (Danio rerio) embryos was served as a model for marine fauna to determine if there is any potential of organ-specific toxicity (neuromuscular, hepatic, cytotoxic, and cardiac) caused by Silicone-Q-22 and Ploy-Q-47. as both surfactants are considered eco-friendly corrosion inhibitors. The calculated LC50 of Silicon-Q-22 and Poly-Q-47 was 22.36 and 8.28 mg/L, respectively. At NOEC both surfactants had resulted in teratogenic defects and cardiotoxicity, but only poly Q-47 resulted in neurotoxicity.

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Звіти організацій з теми "Neurotoxicity assessment"

Jortner, Bernard. Multifactorial Assessment of Depleted Uranium Neurotoxicity. Fort Belvoir, VA: Defense Technical Information Center, October 2004. http://dx.doi.org/10.21236/ada435240.

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Jortner, Bernard S. Multifactorial Assessment of Depleted Uranium Neurotoxicity. Fort Belvoir, VA: Defense Technical Information Center, October 2003. http://dx.doi.org/10.21236/ada419521.

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